Cerebral Blood Flow in Preterm Infants during the First Week of Life

Greisen, Gorm

doi:10.1111/j.1651-2227.1986.tb10155.x

Cited by 162 publications

(73 citation statements)

References 29 publications

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“…Values for CBF and COD were comparable to those previously obtained by NIRS and other techniques (20,21). Because no effect of giving surfactant on these variables could be detected, these results do not suggest that this treatment causes persistent cerebral ischemia, although they do not exclude transient effects.…”

Section: >S Et Alsupporting

confidence: 74%

“…The effects of this therapy on infants immediately after surfactant by a median of -0. 21 intracerebral complications, such as PVH, that lead to later (range -0.46 to 0.05) m L 100 g-I, but quickly recovered morbidity are less certain. Most randomized trials show no so that the median change during the 10 min after surfac-evidence of a change in the incidence of PVH in infants treated tant was 0.01 (-0.46 to 0.46) mL.lOO g-I.…”

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confidence: 99%

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Cerebral Hemodynamic Effects of Treatment with Modified Natural Surfactant Investigated by Near Infrared Spectroscopy

et al. 1992

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ABSTRACT. The purpose of this study was to investigate PAP, peak airway pressure the effects on cerebral hemodynamics of administering EEP, end expiratory pressure modified natural surfactant (Curosurf, to FiOz, inspired oxygen fraction infants requiring mechanical ventilation for hyaline mem-PVH, periventricular cerebral hemorrhage brane disease. Observations were made using near infrared Paoz, arterial oxygen tension spectroscopy on 20 infants for between 26 and 109 (median Pacoz, arterial carbon dioxide tension 57) min before and 22 to 112 (median 46) min after surfactant instillation. Changes in cerebral oxyhemoglobin concentration and cerebral blood volume (CBV) were monitored continuously; cerebral blood flow, oxygen delivery, and the response of CBV to changes in arterial carbonThere is abundant evidence that surfactant replacement therdioxide tension were measured while the infants were apy improves pulmonary gas exchange and reduces mortality in stable shortly before and after surfactant was given. Cere-infants with hyaline membrane disease (surfactant-deficient resbra1 oxyhemoglobin concentration fell transiently in all piratory distress syndrome) (1). The effects of this therapy on infants immediately after surfactant by a median of -0.21 intracerebral complications, such as PVH, that lead to later (range -0.46 to 0.05) m L 100 g-I, but quickly recovered morbidity are less certain. Most randomized trials show no so that the median change during the 10 min after surfac-evidence of a change in the incidence of PVH in infants treated tant was 0.01 (-0.46 to 0.46) mL.lOO g-I. Alterations in with either natural or artificial surfactant (1). However, in one CBV also occurred ranging from -0.44 to 0.40 (median 0) recent multicenter trial in which an enriched extract of bovine mL. 100 g-I, which represented -12 to 16% of total CBV; lung was used, a substantial increase in the incidence of PVH these changes rapidly resolved. When the infants were was found (2). Hemorrhages graded as severe occurred in 39% stable before and after surfactant, the values for mean (SD) of treated infants compared with 15% of controls. Concern about cerebral blood flow were 20.5 (7.5) and 23.1 (5.2) mL. 100 the high incidence of PVH in the treated infants prompted the g-' . min-I, respectively (n = 9); for mean cerebral oxygen U.S. Food and Drug Administration to terminate this trial before delivery, values were 2.71 (0.89) and 3.15 (0.73) mL. 100 planned enrollment was completed. g-' . min-' (n = 9); and for response of CBV to changes in Little information is available about intracerebral consearterial carbon dioxide tension, they were 0.14 (0.09) and quences of surfactant administration that might provoke PVH, 0.11 (0.11) m L 100 g-' . kPa-' (n = 16); these changes although abnormalities of EEG recordings (3) and falls in cerebral were not statistically significant. We conclude that ( I ) arterial blood velocity (4)

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Section: >S Et Alsupporting

confidence: 74%

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confidence: 99%

Cerebral Hemodynamic Effects of Treatment with Modified Natural Surfactant Investigated by Near Infrared Spectroscopy

et al. 1992

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“…The finding of extremely low WM flows is consistent with measurements of mean global CBF in ventilated human premature infants (13)(14)(15)(16)(17)(18)(19). The studies of regional CBF by positron emission tomography showed that values in cerebral WM in surviving preterm infants with normal or near normal neurologic outcome ranged from only 1.6 to 3.0 mL·100 g Ϫ1 ·min Ϫ1 (12).…”

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confidence: 77%

Neurobiology of Periventricular Leukomalacia in the Premature Infant

2001

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Brain injury in the premature infant is a problem of enormous importance. Periventricular leukomalacia (PVL) is the major neuropathologic form of this brain injury and underlies most of the neurologic morbidity encountered in survivors of premature birth. Prevention of PVL now seems ultimately achievable because of recent neurobiologic insights into pathogenesis. The pathogenesis of this lesion relates to three major interacting factors. The first two of these, an incomplete state of development of the vascular supply to the cerebral white matter, and a maturation-dependent impairment in regulation of cerebral blood flow underlie a propensity for ischemic injury to cerebral white matter. The third major pathogenetic factor is the maturation-dependent vulnerability of the oligodendroglial (OL) precursor cell that represents the major cellular target in PVL. Recent neurobiologic studies show that these cells are exquisitely vulnerable to attack by free radicals, known to be generated in abundance with ischemia-reperfusion. This vulnerability of OLs is maturation-dependent, with the OL precursor cell highly vulnerable and the mature OL resistant, and appears to relate to a developmental window characterized by a combination of deficient antioxidant defenses and active acquisition of iron during OL differentiation. The result is generation of deadly reactive oxygen species and apoptotic OL death. Important contributory factors in pathogenesis interact with this central theme of vulnerability to free radical attack. Thus, the increased likelihood of PVL in the presence of intraventricular hemorrhage could relate to increases in local iron concentrations derived from the hemorrhage. The important contributory role of maternal/fetal infection or inflammation and cytokines in the pathogenesis of PVL could be related to effects on the cerebral vasculature and cerebral hemodynamics, to generation of reactive oxygen species, or to direct toxic effects on vulnerable OL precursors. A key role for elevations in extracellular glutamate, caused by ischemia-reperfusion, is suggested by demonstrations that glutamate causes toxicity to OL precursors by both nonreceptor-and receptor-mediated mechanisms. The former involves an exacerbation of the impairment in antioxidant defenses, and the latter, an ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate receptor-mediated cell death. Most importantly, these new insights into the pathogenesis of PVL suggest potential preventive interventions. These include avoidance of cerebral ischemia by detection of infants with impaired cerebrovascular autoregulation, e.g. through the use of in vivo near-infrared spectroscopy, the use of free radical scavengers to prevent toxicity by reactive oxygen species, the administration of ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate receptor antagonists to prevent glutamatemediated injury, or the use of maternal antibiotics or anticytokine agents to prevent toxicity from maternal/fetal infection or inflammation and cytokines.

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“…Xenon clearance, by using inhaled xenon gas, is another technique that is closely related to SPECT and has been extensively used in adults and neonates. 30 Patient motion is a serious limitation of the technique, which, moreover, does not cover the whole brain. The mean CBF with the xenon technique has been estimated at around 50 mL/100 g/min in 7 healthy neonates 31 and 9.5-11.7 mL/100 g/min in 22 preterm infants during the first 3 days of life.…”

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confidence: 99%

Brain Perfusion Imaging in Neonates: An Overview

Proisy

Mitra

Uria-Avellana

et al. 2016

AJNR Am J Neuroradiol

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SUMMARY:The development of cognitive function in children has been related to a regional metabolic increase and an increase in regional brain perfusion. Moreover, brain perfusion plays an important role in the pathogenesis of brain damage in high-risk neonates, both preterm and full-term asphyxiated infants. In this article, we will review and discuss several existing imaging techniques for assessing neonatal brain perfusion. ABBREVIATIONS:ASL ϭ arterial spin-labeling; HIE ϭ hypoxic-ischemic encephalopathy; NIRS ϭ near-infrared spectroscopy

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Cerebral Blood Flow in Preterm Infants during the First Week of Life

Cited by 162 publications

References 29 publications

Cerebral Hemodynamic Effects of Treatment with Modified Natural Surfactant Investigated by Near Infrared Spectroscopy

Cerebral Hemodynamic Effects of Treatment with Modified Natural Surfactant Investigated by Near Infrared Spectroscopy

Neurobiology of Periventricular Leukomalacia in the Premature Infant

Brain Perfusion Imaging in Neonates: An Overview

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